Updated: Jul 20, 2006
Esophageal hematoma is a rare condition that can be spontaneous or secondary to trauma, toxic ingestion, or medical intervention.
Marks and Keet reported a case of a spontaneous intramural hematoma of the esophagus in 1968. This uncommon condition has now been well documented in the literature.
Vomiting can lead to increased intraesophageal pressure that may result in mucosal tears (Mallory-Weiss syndrome), transmural perforation (Boerhaave syndrome), or intramural hematoma of the esophagus. The hemorrhage occurs within submucosal tissues.
Intrinsic esophageal disease, such as achalasia, is rare in patients with esophageal hematoma.
Esophageal hematoma may occur at various sites of the esophagus. The mechanism producing the hematoma may determine the site. For example, a hematoma from vomiting would be in the region of the esophagogastric junction, and a hematoma from a caustic substance might be at points of narrowing.
Approximately 80% of intramural hematomas occur in women.
Primarily middle-aged women are affected. In a literature review of 31 patients, the mean age was 67 years.
A complete and thorough physical examination should be performed.
Esophageal hematomas typically occur in the setting of vomiting or retching, although spontaneous hematomas (more commonly in patients with bleeding disorders) may also occur.
| Boerhaave Syndrome | Myocardial Infarction |
| Esophageal Cancer | Pulmonary Embolism |
| Esophageal Rupture | |
| Esophageal Varices | |
| Mallory-Weiss Tear |
Dissection of the thoracic aorta
Aortoesophageal fistula
For spontaneous intramural hematoma, conservative therapy leads to an excellent prognosis. Esophageal hematomas generally resolve within 2-3 weeks with no long-term sequelae.
Acid suppression by histamine 2 (H2)-receptor antagonists or proton pump inhibitors is useful to treat or prevent esophageal ulcerations.
Inhibit gastric acid secretion by inhibition of the H+/K+/ATP-ase enzyme system in the gastric parietal cells. These agents are used in cases of severe esophagitis and in patients not responding to H2-antagonist therapy.
Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ -ATP pump.
20-40 mg PO qd before breakfast
Not established
May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin
Documented hypersensitivity
C - Safety for use during pregnancy has not been established.
Bioavailability may increase in elderly patients
Inhibits gastric acid secretion. Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers.
30 mg PO qd before breakfast
Not established
May decrease effects of ketoconazole and itraconazole; may increase theophylline clearance
Documented hypersensitivity
B - Usually safe but benefits must outweigh the risks.
Consider adjusting dose in liver impairment. Prolonged treatment (typically > 3 years) may lead to vitamin B12 malabsorption
Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ -ATP pump.
20-mg tab PO qd
Not established
May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin
Documented hypersensitivity
B - Usually safe but benefits must outweigh the risks.
Symptomatic relief with proton pump inhibitors may mask symptoms of gastric malignancy Prolonged treatment (typically > 3 years) may lead to vitamin B12 malabsorption
S-isomer of omeprazole. Inhibits gastric acid secretion by inhibiting H+/K+ -ATP pump at secretory surface of gastric parietal cells.
20-40 mg PO qd
20-40 mg IV qd IV over 10-30 min or by injection over at least three min
Not established
Amoxicillin or clarithromycin may increase plasma levels of esomeprazole when used concurrently; may reduce absorption of dapsone; may increase levels of diazepam and GI absorption of digoxin; may decrease absorption of iron, ketoconazole, and itraconazole
Documented hypersensitivity
C - Safety for use during pregnancy has not been established.
Symptomatic relief with proton pump inhibitors may mask symptoms of gastric malignancy Prolonged treatment (typically > 3 years) may lead to vitamin B12 malabsorption
Inhibits gastric acid secretion by inhibiting H+/K+ -ATP pump at secretory surface of gastric parietal cells.
40 mg PO /IV qd
Not established
May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin
Hypersensitivity to pantoprazole, substituted benzamidazoles (ie, esomeprazole, lansoprazole, omeprazole, rabeprazole), or any component of the formulation
B - Usually safe but benefits must outweigh the risks.
Symptomatic relief with proton pump inhibitors may mask symptoms of gastric malignancy Prolonged treatment (typically > 3 years) may lead to vitamin B12 malabsorption
Reversible competitive blockers of histamine at the H2 receptors, particularly those in the gastric parietal cells where they inhibit acid secretion. The H2 antagonists are highly selective, do not affect the H1 receptors, and are not anticholinergic agents.
Inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which in turn reduces gastric acid secretion, gastric volume, and hydrogen ion concentrations.
150 mg PO bid; not to exceed 600 mg/d
Alternatively, 50 mg/dose IV/IM q6-8h
Not established
May decrease effects of ketoconazole and itraconazole; may alter serum levels of ferrous sulfate, diazepam, nondepolarizing muscle relaxants, and oxaprozin
Documented hypersensitivity
B - Usually safe but benefits must outweigh the risks.
Caution in renal or liver impairment; if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment
Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.
40 mg/d PO bid
Alternatively, 20 mg IV bid
Not established
May decrease effects of ketoconazole and itraconazole
Documented hypersensitivity
B - Usually safe but benefits must outweigh the risks.
If changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment
Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.
300 mg PO hs or 150 mg bid
Not established
None reported
Documented hypersensitivity
C - Safety for use during pregnancy has not been established.
Caution in renal or liver impairment; if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment
Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.
150 mg PO qid; not to exceed 600 mg/d
Alternatively, 50 mg/dose IV/IM q6-8h; not to exceed 400 mg/d
Not established
Can increase blood levels of theophylline, warfarin, tricyclic antidepressants, triamterene, phenytoin, quinidine, propranolol, metronidazole, procainamide, and lidocaine
Documented hypersensitivity
B - Usually safe but benefits must outweigh the risks.
Elderly patients may experience confusional states; may cause impotence and gynecomastia in young males; may increase levels of many drugs; adjust dose or discontinue treatment if changes in renal function occur
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esophageal apoplexy, esophageal mucosal tears, Mallory-Weiss syndrome, transmural perforation, Boerhaave syndrome, intramural hematoma of the esophagus, esophageal perforation, mediastinitis, abscess formation, vomiting, dysphagia, odynophagia, hematemesis, severe acute chest pain
Jennifer Lynn Bonheur, MD, Fellow, Department of Internal Medicine, Division of Gastroenterology, Lenox Hill Hospital
Jennifer Lynn Bonheur, MD is a member of the following medical societies: American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, New York Academy of Sciences, and Sigma Xi
Disclosure: Nothing to disclose.
Klaus Radebold, MD, PhD, Research Associate, Department of Surgery, Yale University School of Medicine
Klaus Radebold, MD, PhD is a member of the following medical societies: American Gastroenterological Association and New York Academy of Sciences
Disclosure: Nothing to disclose.
Maurice A Cerulli, MD, FACG, Chief, Division of Gastroenterology and Hepatology, Associate Professor of Clinical Medicine, Department of Internal Medicine, Division of Gastroenterology, New York Methodist Hospital, Cornell University
Maurice A Cerulli, MD, FACG is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Medical Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Simmy Bank, MD, Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine
Disclosure: Nothing to disclose.
Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.
Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.
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